Repressive coping represents a strategy against threatening information characterized by a general orientation away from threat or minimization of negative emotions. However, when stressed, repressive copers display increased physiological responsiveness compared to nonrepressors. Our own preliminary data suggests that repressive coping is also associated with abnormal lipoprotein profiles, particularly in males compared to females. We hypothesize that these abnormalities are related to elevations in tonic sympathetic-adrenal and pituitary-adrenal activity, to increased physiological stress-responsiveness, and to decreased activity of enzymes related to metabolism of lipids and lipoproteins. Further, we hypothesize that effects of coping style on lipids are not explained by differences in relative body weight, body fat distribution, dietary intake of saturated fat and cholesterol or physical activity. Finally, we expect that coping style effects on lipoprotein profiles will be stable over one year, and that repressive coping may be associated with detrimental lipid changes during periods of stress. To test these hypotheses, 190 male and female medical students, classified according to coping style, will be assessed for levels of serum lipids and lipoproteins and urinary cortisol and catecholamines, four times over one year: twice during stress-free baseline periods and twice during stressful academic examinations. Dietary intake, weight, height and intra-abdominal fat distribution, and physical activity will be measured concurrent with the lipid measurements. Subjects will also be tested for acute cardiovascular responsiveness to a variety of behavioral stressors (speech, mental arithmetic, mirror tracing, isometric exercise), and for activity of the enzymes lipoprotein lipase and hepatic triglyceride lipase at the beginning of the study and again one year later. We expect that male repressors will show increased total and LDL-cholesterols, triglycerides, nonesterified fatty acids, apoliprotein B concentrations, and concommitant increases in urinary cortisol, norepinephrine, epinephrine, and cardiovascular responsiveness during stress, compared to nonrepressors. Identification of individual psychological characteristics and psychophysiological mechanisms which predispose toward lipoprotein abnormalities will have implications for understanding risks for, and prevention and treatment of, atherosclerotic diseases.